This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Hypothesis: We hypothesize that the oncogenic potential of aberrant elevated La protein overstimulates cyclin D1 protein expression and cell proliferation, a hallmark of tumorigenesis in oral cancer. Significance: The poor survival rate of oral cancer patients underscores the need of novel anti-cancer strategies. We propose a novel cellular mechanism, which is a likely contributing factor in oral cancer progression. New insight into the mechanism of cyclin D1 overexpression leads to novel therapeutic interventions, which would be beneficial for many oral cancer patients.